Intracranial Haemorrhages PDF

Intracranial Haemorrhages It is a broad term that refers to bleeding within the cranial cavity caused by ruptures or tears of blood vessels in the cranial cavity and brain (meningeal vessels, dural veins, cerebral arteries). It is a serious medical emergency because the build-up of blood within the...

Intracranial Haemorrhages It is a broad term that refers to bleeding within the cranial cavity caused by ruptures or tears of blood vessels in the cranial cavity and brain (meningeal vessels, dural veins, cerebral arteries). It is a serious medical emergency because the build-up of blood within the skull can lead to an increased in ICP, which can compress delicate brain tissue or limit its blood supply. Severe increases in ICP can cause brain herniation, in which parts of the brain are squeezed past structures in the skull. Trauma is the most common cause of intracranial harmorrhage Classifications of Intracranial Haemorrhages: 1. Extra-axial (outside of brain tissue) haemorrhages a. Epidural harmorrhage b. Subdural harmorrhage (acute and chronic) c. Subarachnoid harmorrhage 2. Intra-axial (inside brain tissue) harmorrhages a. Intracerebral harmorrhage b. Intraventricular haemorrhage Epidural Haemorrhage (accounts for 0.5-1% of all head injuries) Cause: 1. Motor Vehicle Accidents (MVA) 2. Falls 3. Assault 4. Due to direct blunt trauma, causing fractures on the temporal bone Location: Bleeding in the epidural space (a potential space between the skull and the dura mater) Blood vessel: Middle meningeal artery Speed of bleed: Results in rapid worsening of condition as bleeding is arterial Clinical features: 1. Brief LOC due to concussion - 50% wake up after the LOC and have a short “lucid interval: 2. Rapid deterioration of mental status as ICP rises 3. Worsening headache 4. Hemiparesis on opposite side 5. Seizures 6. fixed/dilated pupils on same side 7. If untreated, coma, decerebrate posture, death 8. CT scan: biconvex lens-shaped hyperdense area that does not cross midline. May have midline shift Management: Usually require surgical evacuation of bleed ACUTE Subdural Haemorrhage (more common than epidural haemorrhage) Cause: 1. Motor Vehicle Accidents (MVA) 2. Falls 3. Assault 4. Due to acceleration/deceleration or rotational injuries. May have associated skull fractures Location: Bleed occurs in the subdural space (a potential space between the dura mater and underlying arachnoid mater) Blood vessel: Dural and bridging veins Speed of bleeding: Slower as bleeding is venous Clinical features: 1. Brief LOC due to concussion followed by a relatively longer “lucid interval” 2. Coma again (from increased ICP. 50% present at A&E with coma 3. If untreated, decerebrate rigidity, coma, death 4. Has a bad prognosis if associated with cerebral injury CT Scan: Crescent-shaped hyperdense area that does not cross midline, may have midline shift. Management: Usually requires surgical evacuation of bleed CHRONIC Subdural Haemorrhage (commonly in elderlies >60 years) Cause: 1. Falls or minor injuries which may not be remembered. As brain atrophies shrinks, the bridging veins in dura mater may be torn when there is a rotational or acceleration/deceleration force applied in a fall Location: Occurs in the subdural space Blood vessel: Bridging dural veins Speed of bleed: Slow as bleeding is venous and from a small vein Clinical features: Signs and symptoms may only appear in months and progress slowly after the causative injury because of slow accumulation of venous blood around the atrophied brain 1. Minor headaches (common) 2. Personality changes 3. Fluctuating drowsiness 4. Confusion 5. Weakness 6. Seizure CT Scan: Crescent-shaped hyperdense area that does not cross midline Management: Usually requires surgical evacuation of bleed Subarachnoid Haemorrhage Cause: 1. Blunt trauma 2. acceleration/deceleration injuries 3. Penetrating injuries e.g. gunshot wounds 4. Can be spontaneous from ruptured congenital aneurysm Location: In the subarachnoid space (a real space containing CSF) e.g. around circle of Wills Blood vessel: Cerebral arteries Speed of bleed: Fast as bleeding is arterial Clinical features: 1. Sudden severe headache 2. Vomiting 3. Seizure 4. Deteriorating mental status, LOC 5. Signs of meningism may be present e.g. stiff neck, photophobia CT Scan: Focal hyperdense area in sulci Management: No surgical option. External ventricular drain to reduce ICP. Treat increased ICP and reduce secondary brain injury Pathophysiology of Cerebrovascular Accident (Stroke) Disruption to cerebral blood flow is due to thromboembolism or a ruptured artery, which triggers the ischemic cascade within minutes. Without o2 (due to disrupted blood flow), there will be decreased ATP. With a decreased ATP, Na-K (sodium-potassium) exchange pump fails to function properly causing sodium and water to enter cells, neuronal cell swelling and eventually cerebral edema, which subsequently leads to increased ICP and worsening of the disruption of blood flow. Decreased ATP also causes dysfunction of the Ca++ (calcium) pump which leads to degradation enzyme release that causes inflammation and cell injury. It also leads to glutamate release which excites neighbouring neurons, further depleting ATP. Clinical features: 1. Depends on type of cause (ischemic or hemorrhagic) 2. Cerebral artery involved (anterior, middle or posterior). Presence of good collateral arteries in adjacent areas may reduce the severity 3. State of anastomosis between the internal carotid artery and vertebral artery 4. Middle Cerebral Artery (MCA) most common - 5. Anterior Cerebral Artery (ACA) Infarction 6. Posterior Cerebral Artery (PCA) Infarction Diabetes Mellitus It is a chronic metabolic disorder characterised by the presence of hyperglycaemia due to a deficiency of insulin. It is when the fasting blood glucose is equal or more than 7 mmol/L or HbA1c is more than 6.5 mmmol/mol. The insulin deficiency can be due to: 1. Decreased secretion of insulin 2. Decreased response to insulin 3. Increase in the counter-regulatory hormones (adrenaline, glucocorticoids) Aetiological classifications: , 1. Type 1 DM 2. Type 2 DM 3. Gestational DM 4. Other specific types e.g. a. Pancreatic diseases e.g. pancreatitis b. Endocrine diseases e.g. cushing’s disease, acromegaly c. Drugs e.g. corticosteroids Chronic effects of DM: Chronic increase of blood glucose levels lead to damage to blood vessels (angiopathy) causing basement membranes of blood vessels to thicken and weaken, which result in microvascular complications affecting small vessels e.g. arterioles and capillaries and macrovascular complications, affecting larger vessels e.g. arteries Pathophysiology: In diabetes, decreased insulin prevents glucose from entering cells, leading to hyperglycemia. The body compensates by signalling the liver to increase gluconeogenesis, which worsens the hyperglycemia. Glucosuria occurs as the increased blood glucose load exceeds the capacity of the renal tubular cells to reabrosp glucose. Osmotic diuresis occurs as water follows glucose into the urine. Polyuria arises with compensating polydipsia. Polyphagia results in increased eating as cells are deprived of nutrients. The breakdown of proteins and fats leads to weakness, fatigue and weight loss, while lyposis causes hyperlipidemia and the production of ketones, increases the risk of ketoacidosis Peptic Ulcer Peptic ulcer is an erosion in the mucosal layer part of the gastrointestinal transact that is exposed to acid. It can therefore arise in the oesophagus, stomach or duodonem. *Most (98%) occur in the stomach or duodonem. [*with stomach and duodonem being the most common sites] Duodonel ulcer is the most common type, occurring in the first few cm of the duodonem. It seldom occurs in people with low acid secretion. Gastric ulcer is less common and usually occurs along the lesser curve of the stomach. It may arise from gastritis. Pathophysiology: The stomach’s mucosal lining is normally protected from gastric acid by: Mucus production by the epithelial lining. Mucus prevents contact with acids Bicarbonate produced by the stomach and duodonel cells neutralizes acid, particularly ater meals creating an alkaline tide to buffer the acid surge Prostaglandins has a protective role because it promotes blood flow, mucus production, bicarbonate formation and cell repair Tight junctions between epithelial cells that keep hydrogen ions in the stomach lumen Rapid cell turnover in the epithelial layer. The gastric epithelial has a rapid turnover rate (every 3-4 days), which allows for continuous repair and replacement of damaged cells. Under normal conditions, a balance exists between gastric acid secretion and the five gastroduodenal mucosal defenses. Peptic ulcers develop when this balance is disrupted by aggressive factors like NSAIDs, H. pylori infection, alcohol, and increased acid, which compromise the mucosal defense, allowing hydrogen ions to diffuse into epithelial cells. This causes cell injury, inflammation, and ulcer formation. In duodenal ulcers, H. pylori also impairs duodenal bicarbonate secretion, a defect reversed by eradication of the infection. Increased gastric acid and reduced bicarbonate secretion lower the pH in the duodenum, promoting gastric metaplasia (gastric-type cells in the duodenum). H. pylori infection in metaplastic areas induces duodenitis and increases susceptibility to acid injury, leading to duodenal ulcers. Risk factors: 1. Use of NSAIDs 2. Smoking 3. Alcohol 4. Increased basal acid output and increased maximal acid output 5. Increased gastric emptying Clinical features: Epigastric pain is the most common symptom of both gastric and duodonel ulcers, characterised by gnawing or burning sensation that occurs shortly (almost immediately) after meals with gastric ulcers and 2-3 hours afterward with duodenal ulcers. Patients who develop gastric outlet obstruction as a result of a chronic, untreated duodonel ulcer usually report a history of fullness and bloating associated with nausea and emesis that occurs several hours after food intake Complications: 1. Hemorrhage 2. Perforation 3. Scarring and Stenosis 4. Malignant change Management: Upper GI endoscopy, as it provides the opportunity to visualize the ulcer to determine the presence and degree of active bleeding, and to attempt hemostasis by direct measures if required GIT Bleeding Gastointestinal (GI) bleeding refers to bleeding arising from the GI tract. Bleding from the upper GI tract (oral cavity to small intestines) is 4 times more common than bleeding from the lower GI tract (large intestines to anus) and is a major cause of mordity and mortality. Risk of death from an acute GI bleed is between 5% and 30%. When there is significant blood loss over a short time, symptoms may include hematemesis (vomiting of blood) or melaena (passing out black sticky digested blood in stool) or hematochezia (passing of red blood in the stool). Small amounts of bleeding over a long time is more likely to occur in tumours and the presenting features may be due to iron-deficiency anaemia, such as tiredness, dyspnea, pallor or syncope Causes of GIT bleeding: 1. Oesophagus a. Oesopagitis b. Oesophageal varices c. Oesophageal cancer 2. Stomach a. Gastric ulcer b. Acute erosive gastritis c. Mallory-weiss syndrome d. Stomach cancer 3. Small intestines a. Duodenal ulcer b. Zollinger-Ellison Syndrome c. Meckel’s Diverticulum 4. Large intestines a. Diverticulitis b. Inflammatory Bowel Disease (patients with Chrohn’s disease are not as common as Ulcerative colitis. Ulcerative colitis is more likely to bleed e.g. bloody diarhoea) c. Colorectal cancer d. Hemorrhoids Acute Kidney Injury (AKI) AKI is defined as a sudden or rapid decline in renal filtration function. This usually occurs over hours or days. It manifests as an acute rise in serum creatinine or blood urea nitrogen and oliguria. It results in: 1. Disturbance of ECF volume 2. Electrolyte imbalance (mainly potassium) 3. Acid base abnormalities (metabolic acidosis) 4. Retention of nitrogenous waste products Functions of kidney: 1. Regulates blood, blood pressure 2. Regulates electrolytes (sodium, potassium, calcium, iron) 3. Regulates pH (hydrogen bicarbonate) 4. Excretes toxins, and wastes 5. Produces hormones (renin, EPO, vitamin D) Pathophysiology: AKI due to obstruction results from ischemic injury to renal cells caused by urinary tract blockage, leading to inflammatory responses and tubular cell death. When urine flow is obstructed, it can lead to increased pressure in the renal system, causing ischemia to renal cells. This ischemia triggers inflammation and ultimately results in cell death, contributing to the development of AKI. Aetiology/Causes: 1. Prerenal (most common): As an adaptive response to severe volume depletion and hypotension, with structurally intact nephrons a. Reduced blood volume - Loss of blood from hemorrhage from trauma, surgery, O&G conditions - Loss of plasma in major burns - Loss of water from dehydration in diarrhoea, vomiting, overuse of diuretics, polyuria b. Hypotension from circulatory shock - Hypovolemic shock from haemorrhage, acute pancreatitis - Cardiogenic shock e.g. after AMI, heart failure - Septicemic shock - Anaphylactic shock c. Diseases of major blood vessels - Thrombosis of renal arteries or aorta - Renal arterial stenosis, within the setting of hypotension or initiation of ACE inhibitors or ARBs 2. Intrinsic: In response to cytotoxic, ischemic, or inflammatory insults to the kidney, with structural and functional damage a. Acute tubular necrosis (ATN), either ischemic or cytotoxic b. Toxins e.g. nephroteoxic drugs e.g. aminoglycosides, lithium and radiocontrast agents c. Inflammation of glomerulus e.g. glomerulonephritis d. Pyelonephritis 3. Postrenal (least common): From obstruction to the passage of urine a. Renal obstruction by renal tumours b. Ureteric obstruction by stones c. Accidental surgical cutting of the ureters d. Bladder, urethral obstruction by bladder cancer, benign prostatic hyperplasia (BPH) and urethral structures Clinical features: 1. Oliguric (initiating) phase 2. Maintenance phase 3. Recovery phase